Xu Yu-Dong, Wei Ying, Wang Yu, Yin Lei-Miao, Park Gyoung-Hee, Liu Yan-Yan, Yang Yong-Qing
Shanghai Research Institute of Acupuncture and Meridian, Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Shanghai Research Institute of Acupuncture and Meridian, Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Biochem Biophys Res Commun. 2016 Mar 25;472(1):243-9. doi: 10.1016/j.bbrc.2016.02.098. Epub 2016 Feb 23.
S100A8 is an important member of the S100 protein family, which is involved in intracellular and extracellular regulatory activities. We previously reported that the S100A8 protein was differentially expressed in the asthmatic respiratory tracts. To understand the potential role of S100A8 in asthma, we investigated the effect of recombinant S100A8 protein on the platelet-derived growth factor (PDGF)-induced migration of airway smooth muscle cells (ASMCs) and the underlying molecular mechanism by using multiple methods, such as impedance-based xCELLigence migration assay, transwell migration assays and wound-healing assays. We found that exogenous S100A8 protein significantly inhibited PDGF-induced ASMC migration. Furthermore, the migration inhibition effect of S100A8 was blocked by neutralizing antibody against the receptor for advanced glycation end-products (RAGE), a potential receptor for the S100A8 protein. These findings provide direct evidence that exogenous S100A8 protein inhibits the PDGF-induced migration of ASMCs through the membrane receptor RAGE. Our study highlights a novel role of S100A8 as a potential means of counteracting airway remodeling in chronic airway diseases.
S100A8是S100蛋白家族的重要成员，参与细胞内和细胞外的调节活动。我们之前报道过S100A8蛋白在哮喘呼吸道中存在差异表达。为了解S100A8在哮喘中的潜在作用，我们使用了多种方法，如基于阻抗的xCELLigence迁移试验、Transwell迁移试验和伤口愈合试验，研究重组S100A8蛋白对血小板衍生生长因子（PDGF）诱导的气道平滑肌细胞（ASMCs）迁移的影响及其潜在分子机制。我们发现外源性S100A8蛋白显著抑制PDGF诱导的ASMC迁移。此外，S100A8的迁移抑制作用被抗晚期糖基化终产物受体（RAGE）的中和抗体阻断，RAGE是S100A8蛋白的潜在受体。这些发现提供了直接证据，表明外源性S100A8蛋白通过膜受体RAGE抑制PDGF诱导的ASMC迁移。我们的研究突出了S100A8作为对抗慢性气道疾病中气道重塑的潜在手段的新作用。
